Enhancement of beta-catenin in cardiomyocytes suppresses survival protein expression but promotes apoptosis and fibrosis.

Abstract:

BACKGROUND:Beta-catenin has been implicated in cell-cell communication in a wide variety of developmental and physiological processes. Defective Wnt signaling could result in various cardiac and vascular abnormalities. Little is known regarding Wnt/frizzled pathway in cardiomyocyte apoptosis. METHODS:In this study, the role of b-catenin in apoptosis was investigated in H9c2 cardiomyocytes and primary cardiomyocytes isolated in diabetic Wistar rats. The cardiomyocytes were transfected with porcine cytomegalovirus (pCMV)-b-catenin plasmid in order to overexpress b-catenin. RESULTS:The transcription factor displayed a significant nuclear localization in Wistar rats with cardiac hypertension. Transfection of b-catenin plasmid induced apoptosis and reduced expression of survival pathway markers in cardiomyocytes in a dose-dependent manner. Furthermore, expression of fibrosis protein markers was upregulated by the overexpression. CONCLUSIONS:Taken together, these results revealed that altered Wnt/b-catenin signaling might provoke heart failure. (Cardiol J 2017; 24, 2: 195-205).

journal_name

Cardiol J

journal_title

Cardiology journal

authors

Lin JC,Kuo WW,Baskaran R,Chen MC,Ho TJ,Chen RJ,Chen YF,Vijaya Padma V,Lay IS,Huang CY

doi

10.5603/CJ.a2016.0087

subject

Has Abstract

pub_date

2017-01-01 00:00:00

pages

195-205

issue

2

issn

1897-5593

pii

VM/OJS/J/47776

journal_volume

24

pub_type

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